ArticleCureus2026
Multifocal Uremic Tumoral Calcinosis From Prolonged Hyperparathyroidism in Autosomal Dominant Polycystic Kidney Disease.
Article in Cureus, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper, 1 of them a synthesis that pooled it.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
1 citing paper in PubMed, 1 synthesis or guideline pooled it.
- The cross-cultural and chronological evolution of the kidney-bone relationship: from ancient medical insights to modern molecular endocrinology.Frontiers in endocrinology · 2026Pooled it
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Secondary hyperparathyroidism (SHPT) is a common complication of chronic kidney disease. Prolonged stimulation of the parathyroid glands can lead to severe mineral bone disorders. Uremic tumoral calcinosis (UTC) is a rare but debilitating manifestation of prolonged hyperparathyroidism characterized by periarticular calcium-phosphate deposits. This case describes the progression of SHPT to multifocal UTC in a patient with autosomal dominant polycystic kidney disease (ADPKD). A 46-year-old female with ADPKD-related end-stage renal disease (ESRD) was evaluated for renal transplantation and found to have an elevated parathyroid hormone (PTH) level. A sestamibi scan revealed a left inferior pole parathyroid adenoma, and she underwent a targeted parathyroidectomy. The remaining glands appeared normal intraoperatively and were preserved. Despite optimal medical management after parathyroidectomy, the patient's PTH levels remained markedly elevated. In the ensuing year, the patient developed complications from prolonged hyperparathyroidism, including severe bone pain, arthralgias, pathologic fractures, and multifocal UTC. In ESRD, impaired phosphate excretion and vitamin D metabolism disrupt calcium-phosphate homeostasis, altering the feedback to the parathyroid glands. This leads to chronic elevation of PTH and promotes bone resorption, increasing the risk of pathologic fractures. In some cases, ectopic calcification may occur. Multifocal UTC reflects a severe manifestation of these systemic mineral imbalances. This case illustrates a rare but severe complication of chronic hyperparathyroidism in the setting of ADPKD, where refractory SHPT progressed to multifocal UTC despite surgical and medical interventions. Early recognition and aggressive, multidisciplinary management are critical to mitigate the progression of this condition and preserve quality of life.
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Registered trials
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